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Essential Oils Studied as Protective Agents for Neurological Disorders

Several recent studies have focused on the potential of essential oils to act as protectants to neurological disorders. Some of these studies have focused specifically on the anti-oxidant effects of essential oils, where oxidation (the destruction or alteration of biological molecules by other potentially damaging molecules containing certain forms of oxygen) plays a role. Other [...]

Several recent studies have focused on the potential of essential oils to act as protectants to neurological disorders. Some of these studies have focused specifically on the anti-oxidant effects of essential oils, where oxidation (the destruction or alteration of biological molecules by other potentially damaging molecules containing certain forms of oxygen) plays a role. Other studies have shown that essential oils can keep the mind sharp by preventing the breakdown of Acetylcholine – the primary neurotransmitter involved in the processing of information in the brain.

Essential oils can be used in a number of ways to mimic these studies. Diffusing essential oils has been noted by some researchers to improve test scores in a variety of situations — this effect can potentially be related to the acetylcholine-enhancing properties of the oils. This is the simple diffusion of the oils in the air to the point where their aroma is recognized but not overwhelming. Other studies imply that some oils can be used internally — ie. ingested in small amounts. This of course should only be done with a thorough understanding of the correct dosages (which are VERY small).

Here are two studies that investigate the use of essential oils as antioxidants, and their protective effects on neurons. Other studies involving the acetylcholine neurotransmitter can be found here.

Study: Protective Effects of the Essential Oil of Salvia fruticosa (Greek Sage) and Its Constituents on Astrocytic Susceptibility to Hydrogen Peroxide-Induced Cell Death.

Elmann A, Mordechay S, Rindner M, Larkov O, Elkabetz M, Ravid U. Department of Food Science, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel

Oxidative stress has been implicated in pathologic processes associated with neurodegenerative diseases. Astrocytes, the most abundant glial cell type in the brain, protect neurons from reactive oxygen species (ROS), and any damage to them will affect neuronal survival. This study compares the ability of essential oils prepared from different herbs and spices to protect cultured primary brain astrocytes from H2O2-induced death. The results show that the essential oil of Salvia fruticosa (Sf) among the tested essential oils demonstrated remarkable protective activity. The protective effect of Sf could be attributed to alpha-humulene and alpha-pinene. Following incubation, alpha-humulene and trans-beta-caryophyllene could be found in the cytosol of astrocytes. It is proposed that Sf, by attenuating H2O2-induced cell death, might be used as a functional food or may be offered as a means of therapy in the treatment of neurodegenerative diseases.

Study: Neuroprotective efficacy and therapeutic window of curcuma oil: in rat embolic stroke model.

Dohare P, Garg P, Sharma U, Jagannathan NR, Ray M. Division of Pharmacology, Central Drug Research Institute, PO Box no 173, Chattar Manzil Palace, Lucknow, UP, 226001, India . preetidohare13@gmail.com

BACKGROUND: Among the naturally occurring compounds, turmeric from the dried rhizome of the plant Curcuma longa has long been used extensively as a condiment and a household remedy all over Southeast Asia. Turmeric contains essential oil, yellow pigments (curcuminoids), starch and oleoresin. The present study was designed for investigating the neuroprotective efficacy and the time window for effective therapeutic use of Curcuma oil (C. oil – ed. note: Curcuma or Turmeric essential oil). METHOD: In the present study, the effect of post ischemic treatment of C.oil after ischemia induced by occlusion of the middle cerebral artery in the rat was observed. C.oil (500 mg/kg body wt) was given 4 hrs post ischemia. The significant effect on lesion size as visualized by using diffusion-weighted magnetic resonance imaging and neuroscore was still evident when treatment was started 4 hours after insult. Animals were assessed for behavioral deficit scores after 5 and 24 hours of ischemia. Subsequently, the rats were sacrificed for evaluation of infarct and edema volumes and other parameters. RESULTS: C.oil ameliorated the ischemia induced neurological functional deficits and the infarct and edema volumes measured after 5 and 24 hrs of ischemia. After 24 hrs, immunohistochemical and Western blot analysis demonstrated that the expression of iNOS, cytochrome c and Bax/Bcl-2 were altered after the insult, and antagonized by treatment with C.oil. C.oil significantly reduced nitrosative stress, tended to correct the decreased mitochondrial membrane potential, and also affected caspase-3 activation finally apoptosis. CONCLUSION: Here we demonstrated that iNOS-derived NO produced during ischemic injury was crucial for the up-regulation of ischemic injury targets. C.oil down-regulates these targets this coincided with an increased survival rate of neurons.

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